The contribution of Anísio Teixeira to the promotion of teacher wellbeing

O objetivo o presente artigo consiste em problematizar a contribuição de Anísio Teixeira na promoção da gestão do bem-estar docente. A metodologia empregada para essa investigação é de cunho qualitativo, com coleta de dados na literatura e dados empíricos. A base teórica assenta-se principalmente no legado de Anísio Teixeira, que há mais de meio século já anunciava a vivência desse status nas condições de emprego do professor, bem como sua superação através de uma sólida e continuada formação docente. Os resultados apontam para uma proposta que leve em conta o trabalho colaborativo e a formação de redes intelectuais como forma de superação, e de alcance do bem-estar docente, tão necessário ao desenvolvimento de uma educação de qualidade. Foram encontrados ainda contundentes sinais sobre a responsabilidade da gestão escolar na promoção do bem-estar docente. O diálogo, a escuta e a atitude sensível do gestor foram considerados elementos-chave neste processo. Após a elaboração dessa pesquisa, concluímos que a formação, seja ela inicial ou continuada, a troca com os colegas de profissão, poderá atuar como aliada ao sujeito que está preenchido de algo que faz sentido para sua existência e se alimenta disso como estratégia de superação. A formação continuada, assumida pelos gestores e pelos docentes, surge como um antídoto ao mal-estarThe objective of this paper is to problematize the contribution of Anísio Teixeira in promoting the management of teacher welfare. The methodology used for this research is qualitative, with data collection in the literature and empirical data. The methodology is based mainly on the legacy of Anísio Teixeira, who for more than half a century had already announced the experience of this status in the conditions of employment of the teacher, as well as its overcoming through a solid and continuous training of teachers. The results point to a proposal that considers the collaborative work and the formation of intellectual networks as a way of overcoming, and of reaching the teacher welfare, so necessary to the development of a quality education. Significant signs were also found on the responsibility of school management to promote teacher well-being. The manager's dialogue, listening and sensitive attitude were considered key elements in this process. After the elaboration of this research, we conclude that the formation, be it initial or continued, the exchange with the colleagues of profession, can act as ally to the subject that is filled with something that makes sense for its existence feeds on it as a strategy of overcoming. Continuing education, taken up by managers and teachers, appears as an antidote to malais

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An Investigation in to Virtual World Adoption

Virtual worlds are emerging in importance as more multinational firms are investing heavily in these emerging communities. Although much excitement has been built up around the idea of virtual worlds, a gap exists between those who sign up and those who engage in the virtual world. Our analysis of the gap between those who initiate an action and have signed up to join a virtual world and those who follow through and ultimately engage the community on a regular basis derives from a lack of adoption. Through the use of a subject matter expert study, we identified 35 factors to explain adoption, which then explain through the use of seven psychological theories. After discussing and integrating these seven factors, we test our model through a test of 223 new users of Second Life. The results from our empirical test of these seven theories are presented, and we conclude by discussing the theoretical and practical implications of understanding virtual world adoption

Defining Components of the ßcatenin Destruction Complex and Exploring Its Regulation and Mechanisms of Action during Development

A subset of signaling pathways play exceptionally important roles in embryonic and post-embryonic development, and mis-regulation of these pathways occurs in most human cancers. One such pathway is the Wnt pathway. The primary mechanism keeping Wnt signaling off in the absence of ligand is regulated proteasomal destruction of the canonical Wnt effector ßcatenin (or its fly homolog Armadillo). A substantial body of evidence indicates that SCF(βTrCP) mediates βcat destruction, however, an essential role for Roc1 has not been demonstrated in this process, as would be predicted. In addition, other E3 ligases have also been proposed to destroy βcat, suggesting that βcat destruction may be regulated differently in different tissues.Here we used cultured Drosophila cells, human colon cancer cells, and Drosophila embryos and larvae to explore the machinery that targets Armadillo for destruction. Using RNAi in Drosophila S2 cells to examine which SCF components are essential for Armadillo destruction, we find that Roc1/Roc1a is essential for regulating Armadillo stability, and that in these cells the only F-box protein playing a detectable role is Slimb. Second, we find that while embryonic and larval Drosophila tissues use the same destruction complex proteins, the response of these tissues to destruction complex inactivation differs, with Armadillo levels more elevated in embryos. We provide evidence consistent with the possibility that this is due to differences in armadillo mRNA levels. Third, we find that there is no correlation between the ability of different APC2 mutant proteins to negatively regulate Armadillo levels, and their recently described function in positively-regulating Wnt signaling. Finally, we demonstrate that APC proteins lacking the N-terminal Armadillo-repeat domain cannot restore Armadillo destruction but retain residual function in negatively-regulating Wnt signaling.We use these data to refine our model for how Wnt signaling is regulated during normal development

Irf4-dependent CD103+CD11b+ dendritic cells and the intestinal microbiome regulate monocyte and macrophage activation and intestinal peristalsis in postoperative ileus

Objective: Postoperative ileus (POI), the most frequent complication after intestinal surgery, depends on dendritic cells (DCs) and macrophages. Here, we have investigated the mechanism that activates these cells and the contribution of the intestinal microbiota for POI induction.Design: POI was induced by manipulating the intestine of mice, which selectively lack DCs, monocytes or macrophages. The disease severity in the small and large intestine was analysed by determining the distribution of orally applied fluorescein isothiocyanate-dextran and by measuring the excretion time of a retrogradely inserted glass ball. The impact of the microbiota on intestinal peristalsis was evaluated after oral antibiotic treatment.Results: We found that Cd11c-Cre+ Irf4flox/flox mice lack CD103+CD11b+ DCs, a DC subset unique to the intestine whose function is poorly understood. Their absence in the intestinal muscularis reduced pathogenic inducible nitric oxide synthase (iNOS) production by monocytes and macrophages and ameliorated POI. Pathogenic iNOS was produced in the jejunum by resident Ly6C- macrophages and infiltrating chemokine receptor 2-dependent Ly6C+ monocytes, but in the colon only by the latter demonstrating differential tolerance mechanisms along the intestinal tract. Consistently, depletion of both cell subsets reduced small intestinal POI, whereas the depletion of Ly6C+ monocytes alone was sufficient to prevent large intestinal POI. The differential role of monocytes and macrophages in small and large intestinal POI suggested a potential role of the intestinal microbiota. Indeed, antibiotic treatment reduced iNOS levels and ameliorated POI.Conclusions: Our findings reveal that CD103+CD11b+ DCs and the intestinal microbiome are a prerequisite for the activation of intestinal monocytes and macrophages and for dysregulating intestinal motility in POI

Machine Learning Approaches for the Prediction of Bone Mineral Density by Using Genomic and Phenotypic Data of 5130 Older Men

The study aimed to utilize machine learning (ML) approaches and genomic data to develop a prediction model for bone mineral density (BMD) and identify the best modeling approach for BMD prediction. The genomic and phenotypic data of Osteoporotic Fractures in Men Study (n = 5130) was analyzed. Genetic risk score (GRS) was calculated from 1103 associated SNPs for each participant after a comprehensive genotype imputation. Data were normalized and divided into a training set (80%) and a validation set (20%) for analysis. Random forest, gradient boosting, neural network, and linear regression were used to develop BMD prediction models separately. Ten-fold cross-validation was used for hyper-parameters optimization. Mean square error and mean absolute error were used to assess model performance. When using GRS and phenotypic covariates as the predictors, all ML models’ performance and linear regression in BMD prediction were similar. However, when replacing GRS with the 1103 individual SNPs in the model, ML models performed significantly better than linear regression (with lasso regularization), and the gradient boosting model performed the best. Our study suggested that ML models, especially gradient boosting, can improve BMD prediction in genomic data

Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis

The commensal fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficiency. Although disseminated, vaginal, and oral candidiasis are all caused by C. albicans species, host defense against C. albicans varies by anatomical location. T helper 1 (Th1) cells have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains controversial. IL-17 mediates inflammatory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated disease. Here, we directly compared Th1 and Th17 function in a model of OPC. Th17-deficient (IL-23p19−/−) and IL-17R–deficient (IL-17RA−/−) mice experienced severe OPC, whereas Th1-deficient (IL-12p35−/−) mice showed low fungal burdens and no overt disease. Neutrophil recruitment was impaired in IL-23p19−/− and IL-17RA−/−, but not IL-12−/−, mice, and TCR-αβ cells were more important than TCR-γδ cells. Surprisingly, mice deficient in the Th17 cytokine IL-22 were only mildly susceptible to OPC, indicating that IL-17 rather than IL-22 is vital in defense against oral candidiasis. Gene profiling of oral mucosal tissue showed strong induction of Th17 signature genes, including CXC chemokines and β defensin-3. Saliva from Th17-deficient, but not Th1-deficient, mice exhibited reduced candidacidal activity. Thus, the Th17 lineage, acting largely through IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factors

Policies and Opportunities for Physical Activity in Middle School Environments

This study examined physical activity opportunities and barriers at 36 geographically diverse middle schools participating in the Trial of Activity for Adolescent Girls

Tumor-associated microbiome features of metastatic colorectal cancer and clinical implications

BackgroundColon microbiome composition contributes to the pathogenesis of colorectal cancer (CRC) and prognosis. We analyzed 16S rRNA sequencing data from tumor samples of patients with metastatic CRC and determined the clinical implications.Materials and methodsWe enrolled 133 patients with metastatic CRC at St. Vincent Hospital in Korea. The V3-V4 regions of the 16S rRNA gene from the tumor DNA were amplified, sequenced on an Illumina MiSeq, and analyzed using the DADA2 package.ResultsAfter excluding samples that retained <5% of the total reads after merging, 120 samples were analyzed. The median age of patients was 63 years (range, 34–82 years), and 76 patients (63.3%) were male. The primary cancer sites were the right colon (27.5%), left colon (30.8%), and rectum (41.7%). All subjects received 5-fluouracil-based systemic chemotherapy. After removing genera with <1% of the total reads in each patient, 523 genera were identified. Rectal origin, high CEA level (≥10 ng/mL), and presence of lung metastasis showed higher richness. Survival analysis revealed that the presence of Prevotella (p = 0.052), Fusobacterium (p = 0.002), Selenomonas (p<0.001), Fretibacterium (p = 0.001), Porphyromonas (p = 0.007), Peptostreptococcus (p = 0.002), and Leptotrichia (p = 0.003) were associated with short overall survival (OS, <24 months), while the presence of Sphingomonas was associated with long OS (p = 0.070). From the multivariate analysis, the presence of Selenomonas (hazard ratio [HR], 6.35; 95% confidence interval [CI], 2.38–16.97; p<0.001) was associated with poor prognosis along with high CEA level.ConclusionTumor microbiome features may be useful prognostic biomarkers for metastatic CRC

Two Cases of H2-Receptor Antagonist Hypersensitivity and Cross-Reactivity

H2-receptor antagonists, such as cimetidine, ranitidine and famotidine, are some of the most commonly prescribed medications for gastric acid-related disorders. These compounds are generally well-tolerated and anaphylactic reactions to them are rare. Here, we report two cases of H2-receptor antagonist-induced anaphylactic reactions: the first presented with sudden dyspnea, sneezing, urticaria, and swelling of the eyelids after ranitidine intake. The second presented with sudden severe urticaria, facial swelling, chest discomfort, dizziness, and hypotension. Possible cross-reactivity with other H2-receptor antagonists was assessed by oral challenge and skin tests. To date, only a few reports addressing cross-reactivity among H2-receptor antagonists have been published. We review the literature and summarize the data available on drug cross-reactivity in H2-receptor antagonist hypersensitivity